Search for content and authors

Influence of troglitazone, sodium butyrate and 5-aminosalicylic acid on the chemokine ENA-78/CXCL5 secretion in the intestinal subepithelial myofibroblasts

Arkadiusz R. Gruchlik 1Ewa Chodurek 1Alicja Zajdel 1Adam Wilczok 1Ludmiła Węglarz 2Zofia Dzierżewicz 1

1. Department of Biopharmacy, Medical University of Silesia, Narcyzów 1, Sosnowiec 41-200, Poland
2. Department of Biochemistry, Medical University of Silesia, Narcyzów 1, Sosnowiec 41-200, Poland

Chronic mucosal inflammation is a hallmark of inflammatory bowel disease (IBD). Concentrations of proinflammatory cytokines are noticeably increased in the intestinal mucosa of IBD patients. It has been demonstrated that nuclear factor kappaB (NFkappaB) plays a central role in the regulation of inflammatory signaling pathways in the colon tissue. NFkappaB activates expression of many genes associated with immune function in the gut, e.g. IL-8, IL-6, TNF-α, GM-CSF, and ENA-78/CXCL5 [1]. IL-8 and ENA-78/CXCL5 play complementary and sequential roles in neutrophil recruitment in ulcerative colitis [2]. Fundamental biological processes such as cell motility, proliferation, differentiation, apoptosis, morphogenesis, tissue repair, inflammation, and the immune response in the gut tissue are controlled by myofibroblasts located in the lamina propria under the epithelial cell layer [3].
The present study was aimed at evaluating ENA-78/CXCL5 secretion by human normal colon myofibroblasts CCD-18Co treated with troglitazone (Tro), 5-aminosalicylic acid (5-ASA), sodium butyrate (NaB), and NFκB inhibitor BAY 11–7082.
ENA-78/CXCL5 secretion by TNF-α – stimulated myofibroblasts was evaluated using the commercially available enzyme-linked immunosorbent assay (ELISA) kit. Viability of CCD-18Co cells treated with the chemicals was measured using the XTT tetrazolium salt based assay.
The results showed that 5-ASA, NaB, and BAY 11–7082 decreased ENA-78/CXCL5 secretion in a dose-dependent manner ,while troglitazone (10 - 30 µM) increased secretion of this chemokine by myofibroblasts. All the tested compounds decreased viability of the cells.

[1] Dubuquoy L, Rousseaux C, Thuru X et al. PPARgamma as a new therapeutic target in inflammatory bowel diseases. Gut 2006; 55(9): 1341-1349;
[2] Keates S, Keates AC, Mizoguchi E et al. Enterocytes are the primary source of the chemokine ENA-78 in normal colon and ulcerative colitis. Am J Physiol 1997; 273: 75-82;
[3] Powell DW, Mifflin RC, Valentich JD et al. Myofibroblasts. II. Intestinal subepithelial myofibroblasts. Am J Physiol 1999; 277: 183–201;


Legal notice
  • Legal notice:

Related papers

Presentation: Poster at VII Multidyscyplinarna Konferencja Nauki o Leku, by Arkadiusz R. Gruchlik
See On-line Journal of VII Multidyscyplinarna Konferencja Nauki o Leku

Submitted: 2010-03-15 11:24
Revised:   2010-03-15 11:26